Cardiac work, oxygen use and efficiency
- Concept
- For completeness
The heart spends energy to push blood against pressure. Pumping against high pressure costs far more oxygen than pumping more volume.
Also called: Stroke work, Myocardial oxygen consumption, Tension-time index, Rate–pressure product
See it in 3D: Left ventricle · Ascending aorta
What it is
With each beat the ventricle does external work, mostly pressure–volume work (raising blood to arterial pressure) and a small share as kinetic energy. Its oxygen use depends mainly on wall tension and how long that tension lasts, plus heart rate and contractility. Only about a fifth to a quarter of the chemical energy becomes work; the rest becomes heat.
How it works, step by step
- Energy comes from oxidation: ≈ 70–90% from fatty acids at rest, the rest from lactate and glucose; reserves are tiny, so O₂ use equals energy use.
- Most O₂ is spent building and holding systolic tension, so higher pressure (afterload) raises O₂ use steeply.
- A larger radius needs more tension for the same pressure (Laplace), so a dilated heart spends more O₂ per unit of work.
- Faster rates add more tension periods per minute; positive inotropy raises the cost of each beat.
- Increasing volume at the same pressure uses the Frank–Starling mechanism with little extra tension, so it is cheap.
- Coronary O₂ extraction is already ≈ 70–75% at rest, so extra demand must be met by more coronary flow.
- As arterial pressure rises, the healthy ventricle keeps output nearly constant (it stretches a little and beats harder) until pressure is very high, then output falls.
Left-ventricular pressure–volume loop
EDV 120 mLESV 50 mLSV 70 mLEF 58%ESP 105 mmHg
Normal
Normal loop: EDV about 120 mL, ESV about 50 mL, SV about 70 mL and EF about 60%. The loop's width is the stroke volume and its area is the stroke work.
Tap a corner of the loop (MC, AO, AC, MO) to see the valve event.
- Current loop
- Normal loop
- ESPVR (contractility, Ees)
- EDPVR (passive filling)
- Ea (arterial afterload)
- Stroke volume (SV)
Equations
- SV
- stroke volume
- MAP
- mean arterial pressure
- LVEDP
- left ventricular end-diastolic pressure
Equals the area of the pressure–volume loop; ≈ 1 J per beat for the left ventricle at rest.
- σ
- wall stress
- P
- ventricular pressure
- r
- chamber radius
- h
- wall thickness
Dilation raises stress at the same pressure; hypertrophy (larger h) brings it back down.
- HR
- heart rate
- SBP
- systolic blood pressure
A practical index of myocardial O₂ demand; ≈ 70 × 120 = 8 400 at rest.
Normal ≈ 20–25%.
Reference values (adult at rest)
| Parameter | Value | Note |
|---|---|---|
| Myocardial O₂ use | ≈ 8–10 mL O₂/min per 100 g | |
| Coronary O₂ extraction | ≈ 70–75% | |
| Left ventricular stroke work | ≈ 1 J per beat | |
| Kinetic share of LV work | ≈ 1% | > 50% possible in aortic stenosis |
| Mechanical efficiency | ≈ 20–25% | ≈ 5–10% in heart failure |
| Rate–pressure product | ≈ 7 000–10 000 mmHg/min | angina often at a reproducible value |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Clinical notes
- Hypertension and aortic stenosis load the ventricle with pressure work: hypertrophy, high O₂ demand and angina even with normal coronaries.
- Beta blockers lower heart rate, contractility and systolic pressure, cutting O₂ demand; this is why they help stable angina.
- In stable angina, chest pain often appears at the same rate–pressure product each time: the supply ceiling of a narrowed artery.
Test yourself
Think of the answer, then tap the question to see it.
Two hearts double their stroke work, one by doubling stroke volume and one by doubling pressure. Which uses more O₂, and why?
The pressure-loaded heart. O₂ use follows wall tension × time; raising pressure raises tension in every beat, while raising volume uses the cheap Frank–Starling mechanism.
Why does the kinetic-energy share of left ventricular work rise so much in severe aortic stenosis?
Kinetic energy grows with the square of velocity; blood must pass the narrow valve at very high speed, so a large part of the work goes into accelerating it.
Why does a dilated failing ventricle use more O₂ for the same work?
By Laplace's law, a larger radius needs more wall tension to generate the same pressure, so efficiency falls (to ≈ 5–10%).
A patient's angina starts at a heart rate of 110/min with a systolic pressure of 150 mmHg. What is the rate–pressure product and what does it mean?
16 500 mmHg/min. It estimates the O₂ demand at which supply through the narrowed coronary artery is exceeded; lowering rate or pressure delays angina.
Connections
See it in 3D2
The structures of Durgical's 3D anatomy where it happens.
In Biochemistry2
In Pharmacology1
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: Stable Angina (StatPearls (NCBI Bookshelf), 2025); Aortic Stenosis (StatPearls (NCBI Bookshelf), 2025); Heart Failure (Congestive Heart Failure) (StatPearls (NCBI Bookshelf), 2025).
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Representative model, for educational purposes only.